Secondary hyperparathyroidism and cardiorenal syndrome type iv: Etiopathogenesis, clinical significance and treatment

© 2014, Serbian Medical Society. All rights reserved. Cardiorenal syndrome is a psychophysical disorder of the functions of the heart and kidneys, where the acute or chronic disorder of the functioning of one organ causes the acute or chronic disorder of the functioning of the other organ. In the type 4 of the cardiorenal syndrome (chronic renocardial syndrome), the deficiency of the vitamin D and the secondary hyperparathyroidism cause a disorder of the functioning of the heart and kidneys. The goal of this work is to analyze the risk factors, pathogenetic mechanisms of the development of the secondary hyperparathyroidism and to point out the clinical importance of its early detection and timely treatment. Works written by experts have been examined, as well as the clinical studies researching etiopathogenesis, diagnostics and treatment of secondary hyperparathyroidism. In the chronic kidney disease (stadiums 2 and 3), adaptation mechanisms are activated, while the concentration of FGF-23 and the concentration of parathyroid in the serum both increase. These hormones increase the fractional excretion of the phosphates within the kidney, while parathyroid releases the calcium from the bone tissue, therefore maintaining the concentration of calcium and phosphates in the serum within the normal range. The kidneys' loss of ability to create active vitamin D metabolites and excrete phosphate out of the organism significantly contributes to the development and progress of type 4 cardiorenal syndrome. The main clinical consequences of the secondary hyperparathyroidism are the high turnover bone disease, vascular and valvular calcification and the development of heart diseases. Modern treatment includes the use of phosphate binders that not contain calcium, new vitamin D metabolites and the use of calcimimetics. The early diagnosis and optimal control of secondary hyperparathyroidism prevent the progress of the chronic kidney disease and the development of cardiovascular diseases, reduce the rate of cardiovascular morbidity and mortality and improve the patients' quality of life

Endothelial cell markers from clinician's perspective

Endothelial cell markers are membrane-bound or cytoplasmic molecules expressed by endothelial cells, which help their easier identification and discrimination from other cell types. During vasculogenesis, endothelial cells differentiate from hemangioblasts to form new blood vessels. With the discovery of endothelial progenitor cells (EPC) and their ability to form new blood vessels, the term vasculogenesis is not only reserved for the embryonic development. Possibility of de novo blood vessel formation from EPC is now widely explored in different ischemic conditions, especially in cardiovascular medicine. Numerous clinical trials have tested enhancing tissue vascularization by delivering hematopoietic cells that expressed endothelial markers. This therapeutic approach proved to be challenging and promising, particularly for patients who have exhausted all conventional therapeutic modalities. Angiogenesis, which refers to the formation of new blood vessels from existing vasculature, is indispensable process during tumor progression and metastasis. Blockage of tumor angiogenesis by targeting and inhibiting endothelial cell has emerged as novel safe and efficacious method to control many advanced malignant diseases. Numerous clinical studies are currently testing new antiangiogenic drugs which target and inhibit endothelial cell markers, receptors or molecules which transmit receptor-mediated signals, therefore inhibiting endothelial cell proliferation, migration and vascular tube formation. Many of these drugs are now widely used in clinical settings as first-or second-line chemotherapy in advanced malignant conditions. So far, these therapeutic approaches gave modest, yet encouraging clinical improvements, prolonging survival and improving functional capacity and quality of life for many terminally ill patients. Here we present the most commonly used endothelial cell markers along with their applicability in contemporary clinical practice

Morphometric analysis and redox state of the testicles in nandrolone decanoate and swimming treated adult male rats

Abstract Background During the last decades, the abuse of anabolic androgenic steroids (AASs) has become popular among professional and recreational athletes. The abuse of AASs leads to decreased levels of sex hormones, but the available literature a gives very small pool of data regarding the effects of swimming alone or combined with AASs on testicle tissue. The aim of this study was to investigate the effects of four-week administration of nandrolone decanoate and swimming training alone or in combination on morphometric parameters, androgen receptor (AR) and redox state in testicle tissue. The study included Wistar albino male rats, 10 weeks old, classified into 4 groups: control (T-N-), nandrolone (T-N+), swimming training (T+N-) and swimming training with nandrolone (T+N+). The rats from nandrolone (N+) groups received nandrolone decanoate 20 mg/kg b.w.once per week. The rats from training (T+) groups, swam 1 h/day 5 days/week. The isolated testicles were measured, left testicles were routinely processed for histological analysis, while right testicles were homogenized and prepared for the analysis of the following oxidative stress biomarkers: index of lipid peroxidation (TBARS), nitrites, catalase, superoxide dismutase (SOD), and reduced glutathione (GSH). Results Diameter, as well as cross-section area of seminiferous tubules were decreased by 10 % and 21 % (respectively) in the T-N+ group and by 15% and 41 % (respectively) in the T+N+ group compared to control. Interstitium of the testicles was decreased in all experimental groups. Reduction of immunoreactivity of AR in T-N+ group was 22 %, in T+N+ group was 9 % compared to control. TBARS levels were increased in T+N- and T+N+ groups. Nitrites were decreased in T+N+ group. Catalase activity was increased in all experimental groups. Swimming alone or combined with nandrolone decreased the level of GSH compared to control. SOD activity was decreased in T-N+ and T+N+ groups compared to control. Conclusions Nandrolone alone or combined with swimming decreased morphometric parameters and amount of AR in testicle tissue. Changes in the redox state indicate reproductive dysfunction. </jats:sec